Part One: The story begins with Synapse Action potential travels down the axon and reaches the synaptic bulb. ___ _ _ _ _ _ _ _ _ _ ___ Acetylcholine (ACH) diffuses across the synaptic cleft and binds to receptors. Calcium rushes into pre-synaptic terminal and initiates exocytosis. Electric current from action potential open up voltage gated calcium channels. ACH receptors open the associated gated channels (Na+ gated channels) Na+ rushes through the open channels into the muscle cell causing a large depolarization. Neurotransmitter (from the synaptic vesicles) is released into the cleft. After the initial depolarization of the muscle cell, the muscle cell releases Acetylcholinesterase (ACHE). The electric current in the T-tubules shocks the sarcoplasmic reticulum (opening voltage gated calcium channels) and causes calcium to spill into the cytoplasm of the muscle cell. ACHE begins to destroy the ACH in the synaptic cleft. The wave of depolarization travels along the sarcolemma and down into the T-tubules. When ACH is broken down and unable to bind to the receptors, the Na+ channels close and the depolarization of the muscle cell stops; with no more electric current in the T-tubules, the sarcoplasmic reticulum begins to ‘pick-up’ calcium.

11th Edition

ISBN:9780134580999

Author:Elaine N. Marieb, Katja N. Hoehn

Publisher:Elaine N. Marieb, Katja N. Hoehn

Chapter1: The Human Body: An Orientation

Section: Chapter Questions

Problem 1RQ: The correct sequence of levels forming the structural hierarchy is A. (a) organ, organ system,...

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Part One: The story begins with Synapse

Acetylcholine (ACH) diffuses across the synaptic cleft and binds to receptors.
Calcium rushes into pre-synaptic terminal and initiates exocytosis.
Electric current from action potential open up voltage gated calcium channels.
ACH receptors open the associated gated channels (Na+ gated channels)
Na+ rushes through the open channels into the muscle cell causing a large depolarization.
Neurotransmitter (from the synaptic vesicles) is released into the cleft.
After the initial depolarization of the muscle cell, the muscle cell releases Acetylcholinesterase (ACHE).
The electric current in the T-tubules shocks the sarcoplasmic reticulum (opening voltage gated calcium channels) and causes calcium to spill into the cytoplasm of the muscle cell.
ACHE begins to destroy the ACH in the synaptic cleft.
The wave of depolarization travels along the sarcolemma and down into the T-tubules.
When ACH is broken down and unable to bind to the receptors, the Na+ channels close and the depolarization of the muscle cell stops; with no more electric current in the T-tubules, the sarcoplasmic reticulum begins to ‘pick-up’ calcium.

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Part Two: The rest of the story

Myosin head un-ratchets and is left holding ADP.
As calcium levels in the cytoplasm decrease, there is less calcium to bind troponin and troponin begins to return to its original shape, thus allowing tropomyosin to again cover the actin binding sites.
As long as Actin binding sites are available (and there is ATP available) myosin and actin interaction continues
ATP ‘attaches’ to myosin head, and (via ATP hydrolysis) the energy released allows the myosin head to release the Actin.
Myosin drops the ADP and binds to actin.
The free calcium binds to troponin causing the troponin to change shape.
Myosin heads ratchet, pulling actin towards the M-line.
Troponin’s conformational change (shape change) pulls the tropomyosin off of actin’s binding sites.

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